There has been a global increase in the frequency and spatial scale of red tides. Chattonella spp. which has caused mass mortality of cultured fish in many parts of the world frequently present in coastal waters. C. marina is known to produce high concentrations of reactive oxygen species (ROS), including O2.-, H2O2 and OH.. Several workers therefore, postulated that oxidative stress caused by ROS produced is the main cause of fish-kill by this species. Since ROS is being produced endogenously during aerobic metabolism, a variety of antioxidant enzymes (e.g. superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione reductase (GR)) and free radical scavengers (glutathione (GSH)) have been evolved in aerobic organisms, to remove ROS. However, when these antioxidant responses are overwhelmed by ROS, oxidative damages such as lipid peroxidation (LPO), protein oxidation and DNA-oxidation may occur. We hypothesize that these antioxidant responses will occur when fish is being challenged with oxidative stress caused by C. marina. Using the gold-lined sea bream (Rhabdosargus sarba) as a model, this thesis aims to study: (1) to investigate the responses of antioxidant enzymes and induction of lipid peroxidation in gill and erythrocytes of fish upon exposure to sub-bloom and bloom levels of C. marina, (2) to test the hypothesis that ROS is the main toxic mechanism of C. marina that lead to fish kill, and (3) to explore the possibility of using some of the antioxidant responses as biomarker(s) for oxidative stress induced by C. marina. C. marina produced high levels of H2O2 (9.69 ± 0.19 μM in 2,000 cells/ml and 18.95 ± 1.01 μM in 8,000 cells/ml), which were significantly higher than those in algal (D. tertiolecta) control (~ 1 μM) and seawater control (~ 1 μM). Despite this, no significant changes in antioxidant enzymes, antioxidant scavengers and lipid peroxidation were found in gill and erythrocytes after fish was exposed to high concentration (for 1 & 2 h) and low concentration (for 3 & 6 h) of C. marina. In second part of this study, experiments were also carried out, in which fish were exposed to some 0.5 mM and 1 mM of H2O2 for 1 to 5 h. (equivalent to 25 to 50 times higher than that (~ 20 μM) produced by C. marina). No alterations in SOD was observed in gill, while significant changes in CAT, GPx, GR activities and [GSH]/[GSSG] were observed in the gill upon exposure to 1 mM H2O2 (for 1 & 2 h) and 0.5 mM (for 3 & 5 h). In contrast, no change in GPx, GR activities and [GSH]/[GSSG] were observable in erythrocytes, while SOD and CAT activities in erythrocytes decreased when exposed to both concentrations of H2O2. Lipid peroxidation was not found in both gill and erythrocytes after exposed to 1 mM (for 1 & 2 h) H2O2 and 0.5 mM (for 3 & 5 h). The fact that neither antioxidant response nor lipid peroxidation was found when fish were exposed to C. marina and much higher concentrations of H2O2 provide unequivocal evidence to show that ROS produced by C. marina is not the main cause of ichthyotoxicity in fish kills. A critical analysis of literature data also showed no convincing evidence to suggest that other toxic mechanisms such as impairment of oxygen transfer due to physical gill damage, toxicity caused by production of brevetoxin-like compounds and polyunsaturated fatty acid (PUFA) are involved on fish kill caused by C. marina.